scholarly journals Nano-zinc oxide damages spatial cognition capability via over-enhanced long-term potentiation in hippocamus of Wistar rats

2011 ◽  
pp. 1453 ◽  
Author(s):  
Yang ◽  
Han ◽  
Tian ◽  
Zhang ◽  
Ren
Keyword(s):  
Zinc Oxide ◽  
Spatial Cognition ◽  
Wistar Rats ◽  
Long Term Potentiation ◽  
Nano Zinc Oxide ◽  
Term Potentiation ◽  
Nano Zinc

Intraneuronal [Ca2+] Changes Induced by 2-Deoxy-d-Glucose in Rat Hippocampal Slices

1999 ◽  
Vol 81 (1) ◽  
pp. 174-183 ◽  
Author(s):  
S. Tekkök ◽  
I. Medina ◽  
K. Krnjević
Keyword(s):  
Wistar Rats ◽  
Pyramidal Neurons ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Synergistic Action ◽  
Tetraacetic Acid ◽  
Term Potentiation ◽  
The One ◽  
Peak Increase

Tekkök, S., I. Medina, and K. Krnjević. Intraneuronal [Ca2+] changes induced by 2-deoxy-d-glucose in rat hippocampal slices. J. Neurophysiol. 81: 174–183, 1999. Temporary replacement of glucose by 2-deoxyglucose (2-DG; but not sucrose) is followed by long-term potentiation of CA1 synaptic transmission (2-DG LTP), which is Ca2+-dependent and is prevented by dantrolene or N-methyl-d-aspartate (NMDA) antagonists. To clarify the mechanism of action of 2-DG, we monitored [Ca2+]i while replacing glucose with 2-DG or sucrose. In slices (from Wistar rats) kept submerged at 30°C, pyramidal neurons were loaded with [Ca2+]-sensitive fluo-3 or Fura Red. The fluorescence was measured with a confocal microscope. Bath applications of 10 mM 2-DG (replacing glucose for 15 ± 0.38 min, means ± SE) led to a rapid but reversible rise in fluo-3 fluorescence (or drop of Fura Red fluorescence); the peak increase of fluo-3 fluorescence (Δ F/ F 0), measured near the end of 2-DG applications, was by 245 ± 50% ( n = 32). Isosmolar sucrose (for 15–40 min) had a smaller but significant effect (Δ F/ F 0 = 94 ± 14%, n = 10). The 2-DG–induced Δ F/ F 0 was greatly reduced (to 35 ± 15%, n = 16) by d,l-aminophosphono-valerate (50–100 μM) and abolished by 10 μM dantrolene (−4.0 ± 2.9%, n = 11). A substantial, although smaller effect, of 2-DG persisted in Ca2+-free 1 mM ethylene glycol-bis(β-aminoethyl ether)- N, N, N′, N′-tetraacetic acid (EGTA) medium. Two adenosine antagonists, which do not prevent 2-DG LTP, were also tested; 2-DG–induced Δ F/ F 0 (fluo-3) was not affected by the A1 antagonist 8-cyclopentyl-3,7-dihydro-1,3-dipropyl-1H-purine-2,6-dione (DPCPX 50 nM; 287 ± 38%; n = 20), but it was abolished by the A1/A2 antagonist 8-SPT; 25 ± 29%, n = 19). These observations suggest that 2-DG releases glutamate and adenosine and that the rise in [Ca2+] may be triggered by a synergistic action of glutamate (acting via NMDA receptors) and adenosine (acting via A2b receptors) resulting in Ca2+ release from a dantrolene-sensitive store. The discrepant effects of sucrose and 8-SPT on Δ F/ F 0, on the one hand, and 2-DG LTP, on the other, support other evidence that increases in postsynaptic [Ca2+]i are not essential for 2-DG LTP.

Zinc Oxide and IGZO Bi-layer Synaptic Device with Highly Linear Long-term Potentiation and Depression Characteristics

2021 ◽  
Author(s):  
Hyun-Woong Choi ◽  
Ki-Woo Song ◽  
Seong-Hyun Kim ◽  
Nguyen Kim Thanh ◽  
Sunil Babu Eadi ◽  
...  
Keyword(s):  
Zinc Oxide ◽  
Electrical Properties ◽  
Oxygen Vacancy ◽  
Photoelectron Spectroscopy ◽  
Long Term Potentiation ◽  
Switching Behavior ◽  
Reset Voltage ◽  
Term Potentiation ◽  
Resistance State

Abstract The electrical properties, resistive switching behavior, and long-term potentiation/depression (LTP/LTD) in a single indium-gallium-zinc-oxide (IGZO) and bi-layer IGZO/ZnO memristors were investigated for synapse application. The use of oxide bi-layer memristor, in particular, improved electrical properties such as stability, reliability of memristors, and increase in the synaptic weight states. Bi-layer IGZO/ZnO memristors had a set voltage of 0.9 V, and reset voltage around -0.7 V, resulting in low-power consumption for neuromorphic systems. The oxygen vacancies in X-ray photoelectron spectroscopy analysis played a role in the modulation of the high-resistance state (HRS) (oxygen-deficient) and the low-resistance state (oxygen-rich) region. The VRESET of bi-layer IGZO/ZnO memristors was lower than that of a single IGZO, which implied that oxygen vacancy filaments could be easily ruptured due to the higher oxygen vacancy peak HRS layer. The nonlinearity of LTP and LTD characteristics in a bi-layer IGZO/ZnO memristor was 6.77% and 11.49%, respectively, compared to those of 20.03% and 51.1% in a single IGZO memristor, respectively. Therefore, the extra ZnO layer in the bi-layer memristor with IGZO was potentially significant and essential to achieve a small set voltage and a reset voltage, and the switching behavior to form the conductive path.

Akt3 deletion in mice impairs spatial cognition and hippocampal CA1 long long-term potentiation through downregulation of mTOR

2018 ◽  
Vol 225 (1) ◽  
pp. e13167 ◽  
Author(s):  
Tingting Zhang ◽  
Zhaochun Shi ◽  
Ya Wang ◽  
Ling Wang ◽  
Baofeng Zhang ◽  
...  
Keyword(s):  
Spatial Cognition ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Hippocampal Ca1

Nano-CuO impairs spatial cognition associated with inhibiting hippocampal long-term potentiation via affecting glutamatergic neurotransmission in rats

2018 ◽  
Vol 34 (6) ◽  
pp. 409-421 ◽  
Author(s):  
Xiaoliang Li ◽  
Wei Sun ◽  
Lei An
Keyword(s):  
Spatial Cognition ◽  
Learning And Memory ◽  
Long Term Potentiation ◽  
Copper Oxide Nanoparticles ◽  
Control Group ◽  
Excitatory Postsynaptic Potential ◽  
Potential Health ◽  
Term Potentiation ◽  
Hippocampal Ca1

Manufactured metal nanoparticles and their applications are continuously expanding because of their unique characteristics while their increasing use may predispose to potential health problems. Several studies have reported the adverse effects of copper oxide nanoparticles (nano-CuO) relative to ecotoxicity and cell toxicity, whereas little is known about the neurotoxicity of nano-CuO. The present study aimed to examine its effects on spatial cognition, hippocampal function, and the possible mechanisms. Male Wistar rats were used to establish an animal model, and nano-CuO was administered at a dose of 0.5 mg/kg/day for 2 weeks. The Morris water maze (MWM) test was employed to evaluate learning and memory. The long-term potentiation (LTP) from Schaffer collaterals to the hippocampal CA1 region, and the effects of nano-CuO on synases were recorded in the hippocampal CA1 neurons of rats. MWM test showed that learning and memory abilities were impaired significantly by nano-CuO ( p < 0.05). The LTP test demonstrated that the field excitatory postsynaptic potential (fEPSP) slopes were significantly lower in nano-CuO-treated groups compared with the control group ( p < 0.01). Furthermore, the data of whole-cell patch-clamp experiments showed that nano-CuO markedly depressed the frequencies of both spontaneous excitatory postsynaptic currents (sEPSCs) and miniature EPSCs (mEPSCs), indicating an effect of nano-CuO on inhibiting the release frequency of glutamate presynapticly ( p < 0.01). Meanwhile, the amplitudes of both sEPSC and mEPSC were significantly reduced in nano-CuO-treated animals, which suggested that the effect of nano-CuO modulates postsynaptic receptor kinetics ( p < 0.01). Paired pulse facilitation (PPF) ( p < 0.05) and the expression of NR2A, but not NR2B, of N-methyl-d-aspartate (NMDA) subunits ( p < 0.05), were decreased significantly. In conclusion, nano-CuO impaired glutamate transmission presynapticly and postsynapticly, which may contribute importantly to diminished LTP and other induced cognitive deficits.

scholarly journals Programmable Electrofluidics for Ionic Liquid Based Neuromorphic Platform

Micromachines ◽  
2019 ◽  
Vol 10 (7) ◽  
pp. 478 ◽  
Author(s):  
Walker L. Boldman ◽  
Cheng Zhang ◽  
Thomas Z. Ward ◽  
Dayrl P. Briggs ◽  
Bernadeta R. Srijanto ◽  
...  
Keyword(s):  
Zinc Oxide ◽  
Ionic Liquid ◽  
Long Term Potentiation ◽  
Indium Gallium Zinc Oxide ◽  
Active Matrix ◽  
Von Neumann ◽  
Device Resistance ◽  
Term Potentiation ◽  
Indium Gallium

Due to the limit in computing power arising from the Von Neumann bottleneck, computational devices are being developed that mimic neuro-biological processing in the brain by correlating the device characteristics with the synaptic weight of neurons. This platform combines ionic liquid gating and electrowetting for programmable placement/connectivity of the ionic liquid. In this platform, both short-term potentiation (STP) and long-term potentiation (LTP) are realized via electrostatic and electrochemical doping of the amorphous indium gallium zinc oxide (aIGZO), respectively, and pulsed bias measurements are demonstrated for lower power considerations. While compatible with resistive elements, we demonstrate a platform based on transitive amorphous indium gallium zinc oxide (aIGZO) pixel elements. Using a lithium based ionic liquid, we demonstrate both potentiation (decrease in device resistance) and depression (increase in device resistance), and propose a 2D platform array that would enable a much higher pixel count via Active Matrix electrowetting.

scholarly journals rTMS Ameliorates Prenatal Stress–Induced Cognitive Deficits in Male-Offspring Rats Associated With BDNF/TrkB Signaling Pathway

2019 ◽  
Vol 33 (4) ◽  
pp. 271-283 ◽  
Author(s):  
Yingchun Shang ◽  
Xin Wang ◽  
Fangjuan Li ◽  
Tao Yin ◽  
Jianhai Zhang ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Spatial Cognition ◽  
Cognitive Deficits ◽  
Prenatal Stress ◽  
Long Term Potentiation ◽  
Signaling Proteins ◽  
Ca1 Region ◽  
Hippocampal Synaptic Plasticity ◽  
Term Potentiation

Background. Growing evidences suggest that brain-derived neurotrophic factor/tropomyosin receptor kinase B (BDNF/TrkB) plays a key role in the regulation of hippocampal synaptic plasticity in a prenatal stress (PNS) rat model. Repetitive transcranial magnetic stimulation (rTMS) is currently being acknowledged to affect attention and memory in both preclinical and clinical studies, although the mechanism is still unclear. Objective. The current study aimed to explore whether a whole brain rTMS (5 Hz, 14 days) could ameliorate cognitive dysfunction–induced PNS in male offspring, and examine if the positive effect of rTMS was associated with the BDNF/TrkB signaling in the hippocampus. Methods. The rats were randomly divided into 5 groups: CON, PNS, PNS + rTMS, PNS + rTMS + DMSO (dimethyl sulfoxide), and PNS + rTMS + K252a. Spatial cognition was evaluated by using Morris water maze test. Following behavioral assessment, both paired-pulse facilitation and long-term potentiation were recorded from Schaffer collaterals to CA1 region in the hippocampus. Synaptic, apoptotic, and BDNF/TrkB signaling proteins were measured by Western blot. Results. PNS-exposed offspring exhibited cognitive deficits, long-term potentiation inhibition in the hippocampus, the decrease of synaptic and BDNF/TrkB signaling proteins expression, apoptosis, and reduced number of cells in the CA1 region. Five-hertz rTMS significantly alleviated the PNS-induced abnormalities. However, the effect of rTMS was antagonized by intracerebroventricular infusion of K252a (a TrkB inhibitor). Conclusions. The findings suggest that 5-Hz rTMS significantly improves the impairment of spatial cognition and hippocampal synaptic plasticity, which is possibly associated with the activation of BDNF/TrkB signaling.

scholarly journals Oligomer β-amyloid Induces Hyperactivation of Ras to Impede NMDA Receptor-Dependent Long-Term Potentiation in Hippocampal CA1 of Mice

2020 ◽  
Vol 11 ◽  
Author(s):  
Ya Wang ◽  
Zhaochun Shi ◽  
Yajie Zhang ◽  
Jun Yan ◽  
Wenfeng Yu ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Spatial Cognition ◽  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Small Gtpase ◽  
Ras Activation ◽  
Term Potentiation ◽  
Hippocampal Ca1

The activity of Ras, a small GTPase protein, is increased in brains with Alzheimer’s disease. The objective of this study was to determine the influence of oligomeric Aβ1-42 on the activation of Ras, and the involvement of the Ras hyperactivity in Aβ1-42-induced deficits in spatial cognition and hippocampal synaptic plasticity. Herein, we show that intracerebroventricular injection of Aβ1-42 in mice (Aβ-mice) enhanced hippocampal Ras activation and expression, while 60 min incubation of hippocampal slices in Aβ1-42 (Aβ-slices) only elevated Ras activity. Aβ-mice showed deficits in spatial cognition and NMDA receptor (NMDAR)-dependent long-term potentiation (LTP) in hippocampal CA1, but basal synaptic transmission was enhanced. The above effects of Aβ1-42 were corrected by the Ras inhibitor farnesylthiosalicylic acid (FTS). ERK2 phosphorylation increased, and Src phosphorylation decreased in Aβ-mice and Aβ1-42-slices. Both were corrected by FTS. In CA1 pyramidal cells of Aβ1-42-slices, the response of AMPA receptor and phosphorylation of GluR1 were enhanced with dependence on Ras activation rather than ERK signaling. In contrast, NMDA receptor (NMDAR) function and GluN2A/2B phosphorylation were downregulated in Aβ1-42-slices, which was recovered by application of FTS or the Src activator ouabain, and mimicked in control slices treated with the Src inhibitor PP2. The administration of PP2 impaired the spatial cognition and LTP induction in control mice and FTS-treated Aβ-mice. The treatment of Aβ-mice with ouabain rescued Aβ-impaired spatial cognition and LTP. Overall, the results indicate that the oligomeric Aβ1-42 hyperactivates Ras and thereby causes the downregulation of Src which impedes NMDAR-dependent LTP induction resulting in cognitive deficits.

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